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Gradenigo syndrome as presenting sign of T-cell lymphoma
Gradenigo Syndrome as Presenting Sign of T-Cell Lymphoma Victoria F. Norwood, MD* and Jerome S. Hailer, MDt
Gradenigo syndrome is an uncommonly observed neurologic complex consisting of cranial nerve VI palsy associated with the loss of the sensory component of cranial nerve V. We report a patient whose presentation with Gradenigo syndrome led to the unexpected diagnosis of T-cell lymphoma and briefly discuss Gradenigo syndrome and intracranial lymphomas.
were present bilaterally and facial movements were symmetric. Examination of the remaining cranial nerves was normal. Motor function, peripheral reflexes, gait, and coordination were normal. Because no reproducible neurologic abnormalities were observed, the patient was discharged from the emergency room with analgesics and scheduled for subsequent examination 5 days later. In clinic, he continued to complain of right-sided headache and facial numbness but had the additional complaint of double vision on right lateral gaze. Marked decrease of pinprick sensation of the entire right face, including the mucosa, and loss of the right corneal reflex were demonstrated. Red glass testing confirmed diplopia from a weakness of the right lateral rectus muscle. The remainder of the physical examination was still normal. Enhanced and unenhanced cranial computed tomography (CT) revealed dural enhancement in the medial aspect of the right middle cranial fossa adjacent to the seUa turcica. There was also soft tissue density in the posterior aspect of the right sphenoid sinus and asymmetry of mastoid air cell aeration extending into the petrous bone (Fig 1). Double-dose contrast was given without further definition of the lesion. On magnetic resonance imaging (MRI), the lesion was isodense with gray matter, approximately 1.5 x 4 cm, occupying Meckel's cave and extending into the sphenoid sinus (Fig 2). The right internal carotid artery was compressed and encased by the mass. The proximal segment of the trigeminal nerve was visualized but the
Norwood VF, Hailer JS. Gradenigo syndrome as presenting sign of T-cell lymphoma. Pediatr Neurol 1989;5: 377-80.
Introduction Gradenigo syndrome, first described in 1904, consists of a Vlth nerve palsy and the ipsilateral loss of cranial nerve V sensory components. Classically, this syndrome results from petrositis secondary to middle ear infection. A spaceoccupying lesion is rarely the cause. We report the appearance of Gradenigo syndrome as the first manifestation of T-cell lymphoma in a child.
Case Report This 13-year-old black male presented to the pediatric emergency room at Charity Hospital of New Orleans with a 7-day history of headache described as right-sided, throbbing pain, posterior to the eye, and associated with right-sided facial numbness. He complained of anorexia and nausea but no vomiting or dysphagia. There were no visual changes or disturbances. Sinusitis was diagnosed at another hospital, but treatment with ampicillin and antihistamine/decongestant was ineffective. His medical history was unremarkable. With the exception of the neurologic findings, the physical examination was normal. Although appearing in pain, he was cooperative and had an intact mental status. He reported right-sided loss of vibratory sense to the face and split the midline to tuning fork examination. He appeared to have decreased sensation of light touch to the entire right face; pinprick was equivocal on the face and in the oral cavity. Pupils were equal and briskly reactive and discs were sharp. Extraocular movements were full and bite strength was excellent. Corneal reflexes
From the *Department of Pediatrics; Tulane University School of Medicine; New Orleans, Louisiana; tDepartment of Neurology, Section of Child Neurology; Albany Medical Center; Albany, New York.
Figure 1. CT revealing a slightly enhanced lesion anterior to the right petrous ridge (large arrows). Asymmetry of the mastoid air cells (small arrow) and a mass lesion in the right sphenoid sinus (arrowhead) are observed.
Communications should be addressed to: Dr. Norwood; Department of Pediatrics; Tulane University School of Medicine; 1430 Tulane Avenue; New Orleans, LA 70112. Received June 14, 1989; accepted October 10, 1989.
Norwood and Hailer: T-Cell Lymphoma 377
Figure 2. MRI sagittal section demonstrating a mass lesion in the posterior aspect of the sphenoid sinus (arrow). Meckel's cave segment was obliterated by the mass. Coronal sections documented the site of the tumor as extradural (Fig 3). Because of the continuity between the intracranial mass and the density in the sphenoid sinus, a transsphenoidal biopsy was performed and the diagnosis of T-cell lymphoma, Lennert type, was determined (Fig 4). Further evaluation revealed diffuse involvement of bone marrow, spleen, kidneys, and testes with T-cell lymphoma. Immunologic workup revealed an unexpected common variable, hypogammaglobulinemia with decreased IgG, IgM, and IgA. The child underwent combination chemotherapy and radiotherapy with complete resolution of all symptoms and signs. He is doing well on consolidation chemotherapy.
types. They classically present with an anterior m e d i c a l mass with or without peripheral lymphadenopathy, although all combinations of nodal and extranodal Sites are possible. These tumors occur predominantly in older children and young adolescents with a high male.to-female ratio. Evaluation of central nervous system (CNS) involvement in non-Hodgkin's lymphoma is the subject of much study and is complicated by frequent changes in nomen.
Discussion Gradenigo syndrome, first described in 1904, consists of cranial nerve VI palsy and abnormalities of the sensory component of ipsilateral cranial nerve V. Gradenigo observed the symptom complex in association with middle ear infections and concluded that it was "the result of a circumscribed purulent or simple serous leptomeningitis localized about the tip of the petrous pyramid and caused by the diffusion of the infection in the tympanum" [1]. He reported that the symptoms usually resolved spontaneously or with treatment of the tympanic membrane or mastoid infection, although some patients died as a result of meningitis. Gradenigo syndrome also has been reported as the result of a space-occupying lesion, most commonly a neurofibroma. With the advent of modem antibiotic therapy, the eradication of the most severe complications of otitis media has made Gradenigo syndrome a rare entity. T-cell lymphoma, anterior to the petrous ridge impinging on cranial nerves V and VI, represents a most unusual etiology for this syndrome. Childhood T-cell lymphomas are referred to as both lymphoblastic and poorly differentiated lymphocytic
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Figure 3. MRI coronal section demonstrating a mass lesion medial to the right temporal lobe (large arrow) extending into the sphenoid sinus (small arrow),
Figure 4. Histologic section of the sphenoid mass revealing the lymphomatous process. The great number of histiocytes with an epithelioid pattern, as well as immunoblastic mononuclear cells, establish the pattern of Lennert lymphoma.
clature of tumor subtypes; however, there are two basic subgroups of CNS lymphoma: primary involvement of the brain or secondary spread from disseminated disease. Primary CNS lymphoma without systemic involvement is quite rare, comprising 0.3-2.3% of all intracranial neoplasms [2,3] and approximately 2% of all lymphomas [4]. It occurs most commonly in organ transplant patients or in patients with primary immunodeficiencies, although larger numbers of cases in normal hosts have recently been reported. The most frequent reports of immunodeficiencies involve patients with Wiskott-Aldrich syndrome in whom up to 40% may develop primary CNS lymphoma [5]. Patients with HTLV I and III infections, ataxia-telangiectasia, X-linked agammaglobulinemia, severe combined immunodeficiency, common variable immunodeficiency, and IgA deficiency are also at risk [6]. Evaluation of our patient's immune function revealed a previously unsuspected hypogammaglobulinemia. Primary CNS lymphomas are most commonly of B-cell origin as determined by monoclonal antibody studies [3,6]. Most commonly, primary CNS lymphomas present as a discrete single or multiple intraparenchymal lesions, less commonly as meningeal and spinal cord tumors [6]. Supratentorial lesions predominate; however, some authors report a high incidence of involvement of the basal structures [7]. In general, patients present with signs of increased intracranial
pressure or mental status change. Focal signs, including cranial nerve abnormalities, may also be observed [4]. The second form of CNS involvement with lymphoma occurs as a part of a generalized systemic disease. Incidence figures of CNS involvement range from 10% or higher, depending on the histologic subgroup [8,9]. Watanabe et al. reported that 48% of children with bone marrow involvement from undifferentiated lymphoma develop meningeal involvement, some prior to bone marrow transformation [9]. The pathologic lesion is usually that of leptomeningitis though focal cerebral lesions and spinal cord compression can occur [ 10]. Presenting signs of cranial nerve findings, usually facial nerve palsy, are fairly common. Secondary CNS lymphoma may occur at any time in the patient's clinical course, but is usually found with poorly controlled progressive disease and may signal systemic relapse [l l]. Progression to CNS lymphoma is an expected course for adolescents with T-cell disease presenting with a mediastinal mass [ 12]. Our patient's tumor classification of Lennert T-cell lymphoma is another unusual aspect of childhood nonHodgkin's lymphomas. "Lennert lymphoma" was first described in 1968 as a variant of Hodgkin's disease. Since that time, it also has been described in association with non-Hodgkin's lymphoma and other rare lymphoid abnormalities. Usually the disease manifests in older patients with a history of allergies and hypergammaglobulinemia and presents with lymphadenopathy. A few patients have had nasopharyngeai masses [13]. Histologically, the lesions have a high percentage of epithelioid cells; recent evaluation by immunohistochemical technique documented a high percentage of T-cell markers [14]. To our knowledge, this is the first report of childhood Lennert lymphoma and the first report of this lymphoma presenting with CNS changes. This report represents an interesting point along the spectrum of lymphomatous disease. Designation of the intracranial lesion as primary or secondary appears impossible because it was the only true mass lesion in the presence of disseminated lymphoma. Schaumberg et al. described 2 patients with sphenoid/intrasellar tumors extending into the basal structures of the brain (one with systemic disease, one not classified) and 3 patients with epidural tumors which appeared to arise from bony lesions [ 15]. All 5 patients were previously known to have systemic disease. These patients all had some element of cranial nerve involvement but none with the cranial nerve V and VI combination of Gradenigo syndrome [15]. The primary neurologic presentation of T-cell Lennert lymphoma has never been described previously. An intracranial lesion as a presenting sign of systemic disease is quite unusual and the involvement of cranial nerves V and VI provide an interesting new etiology for Gradenigo syndrome. The authors would like to thank Dr. Syed Hoda for his assistance with preparation and retrieval of the histopathologic specimens.
Norwood and Hailer: T-Cell Lymphoma 379
References
111 Gradenigo G. A special syndrome of endocranial otitic complications. Ann Otol Rhinol Laryngol 1904;13:637-8. [2] Jellinger K, Radaskiewicz T, Slowik F. Primary malignant lymphomas of the central nervous system in man. Acta Neuropathol 1975; 6:95-102. [3] Spaun E, Midholm S, Pedersen NT, Ringsted J. Primary malignant lymphoma of the central nervous system. Surg Neurol 1985;24: 646-50. [4] Woodman R, Shin K, Pineo G. Primary non-Hodgkin's lymphoma of the brain. Medicine 1985;64:425-30. [5] Penn I. Depressed immunity and the development of cancer. Clin Exp Immunol 1981;46:459-74. [6] Bogdahn U, Bogdahn S, Mertens HG, et al. Primary nonHodgkin's lymphomas of the CNS. Acta Neurol Scand 1986;73:602-14. [7] SpiUane JA, Kendall BE, Moseley IF. Cerebral lymphoma: Clinical radiological correlation. J Neurol Neurosurg Psychiatry 1982; 45:199-208. [81 Nathwani BN, Kim H, Rappaport H. Malignant lymphoma, lymphoblastic. Cancer 1976;38:964-83.
380 PEDIATRIC NEUROLOGY
Vol. 5 No. 6
[91 Watanabe A, Sullivan ME Sutow WW. Wilbur JR I]~diOk'ren tiated lymphoma, non-Burkitt's type. Am J [)is Child 1c,~73:[25:57-61 [10] Young RC, ltowser DM, Anderson T, f:ischcr RI, ,hdie E, DeVita VT. Central nervous system complication~ ¢~1'nnn-Hodgkin's lymphoma. Am J Med 1979;66:435-43. [11] Levitt LJ, Dawson DM, Rosenthal DS. Moloney WC. CNS involvement in the non-Hodgkin's lymphomas. Cancer 1980:45:545-52 [12] Jones SE. Non-Hodgkin's lymphnmas. J A M A 1975:234:633-8. [13] Burke JS, Butler JJ. Malignant lymphoma with a high content of epithelioid histiocytes (Lennert's lymphoma). Am .1 Clin Pathol 1976:66:1-9. [14] Feller AC, Griesser GH, Mak TW, Lennert K. Lympho-epithelioid lymphoma (Lennert's lymphoma) is a monoclonal proliferation of helper/inducer T Cells. Blood 1986;68:663-7. [15] Sehaumbnrg HH, Plank CR, Adams RD. The reticulum cell sarcoma-microglioma group of brain tumors. Brain 1972;95: I¢)9-212.
Gradenigo syndrome is an uncommonly observed neurologic complex consisting of cranial nerve VI palsy associated with the loss of the sensory component of cranial nerve V. We report a patient whose presentation with Gradenigo syndrome led to the unexpected diagnosis of T-cell lymphoma and briefly discuss Gradenigo syndrome and intracranial lymphomas.
were present bilaterally and facial movements were symmetric. Examination of the remaining cranial nerves was normal. Motor function, peripheral reflexes, gait, and coordination were normal. Because no reproducible neurologic abnormalities were observed, the patient was discharged from the emergency room with analgesics and scheduled for subsequent examination 5 days later. In clinic, he continued to complain of right-sided headache and facial numbness but had the additional complaint of double vision on right lateral gaze. Marked decrease of pinprick sensation of the entire right face, including the mucosa, and loss of the right corneal reflex were demonstrated. Red glass testing confirmed diplopia from a weakness of the right lateral rectus muscle. The remainder of the physical examination was still normal. Enhanced and unenhanced cranial computed tomography (CT) revealed dural enhancement in the medial aspect of the right middle cranial fossa adjacent to the seUa turcica. There was also soft tissue density in the posterior aspect of the right sphenoid sinus and asymmetry of mastoid air cell aeration extending into the petrous bone (Fig 1). Double-dose contrast was given without further definition of the lesion. On magnetic resonance imaging (MRI), the lesion was isodense with gray matter, approximately 1.5 x 4 cm, occupying Meckel's cave and extending into the sphenoid sinus (Fig 2). The right internal carotid artery was compressed and encased by the mass. The proximal segment of the trigeminal nerve was visualized but the
Norwood VF, Hailer JS. Gradenigo syndrome as presenting sign of T-cell lymphoma. Pediatr Neurol 1989;5: 377-80.
Introduction Gradenigo syndrome, first described in 1904, consists of a Vlth nerve palsy and the ipsilateral loss of cranial nerve V sensory components. Classically, this syndrome results from petrositis secondary to middle ear infection. A spaceoccupying lesion is rarely the cause. We report the appearance of Gradenigo syndrome as the first manifestation of T-cell lymphoma in a child.
Case Report This 13-year-old black male presented to the pediatric emergency room at Charity Hospital of New Orleans with a 7-day history of headache described as right-sided, throbbing pain, posterior to the eye, and associated with right-sided facial numbness. He complained of anorexia and nausea but no vomiting or dysphagia. There were no visual changes or disturbances. Sinusitis was diagnosed at another hospital, but treatment with ampicillin and antihistamine/decongestant was ineffective. His medical history was unremarkable. With the exception of the neurologic findings, the physical examination was normal. Although appearing in pain, he was cooperative and had an intact mental status. He reported right-sided loss of vibratory sense to the face and split the midline to tuning fork examination. He appeared to have decreased sensation of light touch to the entire right face; pinprick was equivocal on the face and in the oral cavity. Pupils were equal and briskly reactive and discs were sharp. Extraocular movements were full and bite strength was excellent. Corneal reflexes
From the *Department of Pediatrics; Tulane University School of Medicine; New Orleans, Louisiana; tDepartment of Neurology, Section of Child Neurology; Albany Medical Center; Albany, New York.
Figure 1. CT revealing a slightly enhanced lesion anterior to the right petrous ridge (large arrows). Asymmetry of the mastoid air cells (small arrow) and a mass lesion in the right sphenoid sinus (arrowhead) are observed.
Communications should be addressed to: Dr. Norwood; Department of Pediatrics; Tulane University School of Medicine; 1430 Tulane Avenue; New Orleans, LA 70112. Received June 14, 1989; accepted October 10, 1989.
Norwood and Hailer: T-Cell Lymphoma 377
Figure 2. MRI sagittal section demonstrating a mass lesion in the posterior aspect of the sphenoid sinus (arrow). Meckel's cave segment was obliterated by the mass. Coronal sections documented the site of the tumor as extradural (Fig 3). Because of the continuity between the intracranial mass and the density in the sphenoid sinus, a transsphenoidal biopsy was performed and the diagnosis of T-cell lymphoma, Lennert type, was determined (Fig 4). Further evaluation revealed diffuse involvement of bone marrow, spleen, kidneys, and testes with T-cell lymphoma. Immunologic workup revealed an unexpected common variable, hypogammaglobulinemia with decreased IgG, IgM, and IgA. The child underwent combination chemotherapy and radiotherapy with complete resolution of all symptoms and signs. He is doing well on consolidation chemotherapy.
types. They classically present with an anterior m e d i c a l mass with or without peripheral lymphadenopathy, although all combinations of nodal and extranodal Sites are possible. These tumors occur predominantly in older children and young adolescents with a high male.to-female ratio. Evaluation of central nervous system (CNS) involvement in non-Hodgkin's lymphoma is the subject of much study and is complicated by frequent changes in nomen.
Discussion Gradenigo syndrome, first described in 1904, consists of cranial nerve VI palsy and abnormalities of the sensory component of ipsilateral cranial nerve V. Gradenigo observed the symptom complex in association with middle ear infections and concluded that it was "the result of a circumscribed purulent or simple serous leptomeningitis localized about the tip of the petrous pyramid and caused by the diffusion of the infection in the tympanum" [1]. He reported that the symptoms usually resolved spontaneously or with treatment of the tympanic membrane or mastoid infection, although some patients died as a result of meningitis. Gradenigo syndrome also has been reported as the result of a space-occupying lesion, most commonly a neurofibroma. With the advent of modem antibiotic therapy, the eradication of the most severe complications of otitis media has made Gradenigo syndrome a rare entity. T-cell lymphoma, anterior to the petrous ridge impinging on cranial nerves V and VI, represents a most unusual etiology for this syndrome. Childhood T-cell lymphomas are referred to as both lymphoblastic and poorly differentiated lymphocytic
378
PEDIATRIC NEUROLOGY
Vol. 5 No. 6
Figure 3. MRI coronal section demonstrating a mass lesion medial to the right temporal lobe (large arrow) extending into the sphenoid sinus (small arrow),
Figure 4. Histologic section of the sphenoid mass revealing the lymphomatous process. The great number of histiocytes with an epithelioid pattern, as well as immunoblastic mononuclear cells, establish the pattern of Lennert lymphoma.
clature of tumor subtypes; however, there are two basic subgroups of CNS lymphoma: primary involvement of the brain or secondary spread from disseminated disease. Primary CNS lymphoma without systemic involvement is quite rare, comprising 0.3-2.3% of all intracranial neoplasms [2,3] and approximately 2% of all lymphomas [4]. It occurs most commonly in organ transplant patients or in patients with primary immunodeficiencies, although larger numbers of cases in normal hosts have recently been reported. The most frequent reports of immunodeficiencies involve patients with Wiskott-Aldrich syndrome in whom up to 40% may develop primary CNS lymphoma [5]. Patients with HTLV I and III infections, ataxia-telangiectasia, X-linked agammaglobulinemia, severe combined immunodeficiency, common variable immunodeficiency, and IgA deficiency are also at risk [6]. Evaluation of our patient's immune function revealed a previously unsuspected hypogammaglobulinemia. Primary CNS lymphomas are most commonly of B-cell origin as determined by monoclonal antibody studies [3,6]. Most commonly, primary CNS lymphomas present as a discrete single or multiple intraparenchymal lesions, less commonly as meningeal and spinal cord tumors [6]. Supratentorial lesions predominate; however, some authors report a high incidence of involvement of the basal structures [7]. In general, patients present with signs of increased intracranial
pressure or mental status change. Focal signs, including cranial nerve abnormalities, may also be observed [4]. The second form of CNS involvement with lymphoma occurs as a part of a generalized systemic disease. Incidence figures of CNS involvement range from 10% or higher, depending on the histologic subgroup [8,9]. Watanabe et al. reported that 48% of children with bone marrow involvement from undifferentiated lymphoma develop meningeal involvement, some prior to bone marrow transformation [9]. The pathologic lesion is usually that of leptomeningitis though focal cerebral lesions and spinal cord compression can occur [ 10]. Presenting signs of cranial nerve findings, usually facial nerve palsy, are fairly common. Secondary CNS lymphoma may occur at any time in the patient's clinical course, but is usually found with poorly controlled progressive disease and may signal systemic relapse [l l]. Progression to CNS lymphoma is an expected course for adolescents with T-cell disease presenting with a mediastinal mass [ 12]. Our patient's tumor classification of Lennert T-cell lymphoma is another unusual aspect of childhood nonHodgkin's lymphomas. "Lennert lymphoma" was first described in 1968 as a variant of Hodgkin's disease. Since that time, it also has been described in association with non-Hodgkin's lymphoma and other rare lymphoid abnormalities. Usually the disease manifests in older patients with a history of allergies and hypergammaglobulinemia and presents with lymphadenopathy. A few patients have had nasopharyngeai masses [13]. Histologically, the lesions have a high percentage of epithelioid cells; recent evaluation by immunohistochemical technique documented a high percentage of T-cell markers [14]. To our knowledge, this is the first report of childhood Lennert lymphoma and the first report of this lymphoma presenting with CNS changes. This report represents an interesting point along the spectrum of lymphomatous disease. Designation of the intracranial lesion as primary or secondary appears impossible because it was the only true mass lesion in the presence of disseminated lymphoma. Schaumberg et al. described 2 patients with sphenoid/intrasellar tumors extending into the basal structures of the brain (one with systemic disease, one not classified) and 3 patients with epidural tumors which appeared to arise from bony lesions [ 15]. All 5 patients were previously known to have systemic disease. These patients all had some element of cranial nerve involvement but none with the cranial nerve V and VI combination of Gradenigo syndrome [15]. The primary neurologic presentation of T-cell Lennert lymphoma has never been described previously. An intracranial lesion as a presenting sign of systemic disease is quite unusual and the involvement of cranial nerves V and VI provide an interesting new etiology for Gradenigo syndrome. The authors would like to thank Dr. Syed Hoda for his assistance with preparation and retrieval of the histopathologic specimens.
Norwood and Hailer: T-Cell Lymphoma 379
References
111 Gradenigo G. A special syndrome of endocranial otitic complications. Ann Otol Rhinol Laryngol 1904;13:637-8. [2] Jellinger K, Radaskiewicz T, Slowik F. Primary malignant lymphomas of the central nervous system in man. Acta Neuropathol 1975; 6:95-102. [3] Spaun E, Midholm S, Pedersen NT, Ringsted J. Primary malignant lymphoma of the central nervous system. Surg Neurol 1985;24: 646-50. [4] Woodman R, Shin K, Pineo G. Primary non-Hodgkin's lymphoma of the brain. Medicine 1985;64:425-30. [5] Penn I. Depressed immunity and the development of cancer. Clin Exp Immunol 1981;46:459-74. [6] Bogdahn U, Bogdahn S, Mertens HG, et al. Primary nonHodgkin's lymphomas of the CNS. Acta Neurol Scand 1986;73:602-14. [7] SpiUane JA, Kendall BE, Moseley IF. Cerebral lymphoma: Clinical radiological correlation. J Neurol Neurosurg Psychiatry 1982; 45:199-208. [81 Nathwani BN, Kim H, Rappaport H. Malignant lymphoma, lymphoblastic. Cancer 1976;38:964-83.
380 PEDIATRIC NEUROLOGY
Vol. 5 No. 6
[91 Watanabe A, Sullivan ME Sutow WW. Wilbur JR I]~diOk'ren tiated lymphoma, non-Burkitt's type. Am J [)is Child 1c,~73:[25:57-61 [10] Young RC, ltowser DM, Anderson T, f:ischcr RI, ,hdie E, DeVita VT. Central nervous system complication~ ¢~1'nnn-Hodgkin's lymphoma. Am J Med 1979;66:435-43. [11] Levitt LJ, Dawson DM, Rosenthal DS. Moloney WC. CNS involvement in the non-Hodgkin's lymphomas. Cancer 1980:45:545-52 [12] Jones SE. Non-Hodgkin's lymphnmas. J A M A 1975:234:633-8. [13] Burke JS, Butler JJ. Malignant lymphoma with a high content of epithelioid histiocytes (Lennert's lymphoma). Am .1 Clin Pathol 1976:66:1-9. [14] Feller AC, Griesser GH, Mak TW, Lennert K. Lympho-epithelioid lymphoma (Lennert's lymphoma) is a monoclonal proliferation of helper/inducer T Cells. Blood 1986;68:663-7. [15] Sehaumbnrg HH, Plank CR, Adams RD. The reticulum cell sarcoma-microglioma group of brain tumors. Brain 1972;95: I¢)9-212.